Atrioventricular blocks are either a conduction delay or a complete block of impulses from the atria to the ventricles. They may be caused by a variety of things ranging from athletic training to pain or stimulation of the carotid sinus.
o First degree AV block is a measurement of conduction time between the atria and the ventricles and is represented by the PR interval. It includes the P wave as well. A PR interval o more than 200 millisecond is considered a first-degree AV block. Causes include structural abnormalities, increased vagal tone and drug use (i.e., digoxin, beta blockers, and calcium channel inhibitors).
o A second-degree atrioventricular block includes occasional non-conducted P waves with prolonged PR intervals. It is characterized by an absent impulse not the ventricles and reflects a disappearance of the QRS complex.
o Second-Degree AV Block Type 1
o Gradual lengthening of PR interval occurs due to prolonged AV conduction time initial an atrial impulse is unconducted and a QRS complex is blocked. May result from drugs (digoxin or beta blockers) or CAD. Atrial rate regular but ventricle rate is slower resulting in bradycardia. P wave and QRS complex are normal. Usually a result of myocardial ischemia or inferior MI, transient and well tolerated. Sometimes it may be a warning sign of an acute MI. If pt is symptomatic atropine is used to increase HR or pacemaker is needed. If pt is asymptomatic the rhythm is monitored using transcutaneous pacemaker. Bradycardia is more likely to become symptomatic when hypotension, HF, or shock are present.
o Second-Degree AV Block Type 2
o P wave is non-conducted without progressive PR lengthening. On conducted beats, the PR interval is constant. More serious type of block in which a certain number of impulses from the SA node are not conducted to the ventricles. Associated with rheumatic heart disease, CAD, anterior MI, and drug toxicity. Atrial rate normal, ventricular rate depends on degree of block. Atrial rhythm normal, ventricular rhythm may be irregular. P wave normal shape, PR may be normal or prolonged. QRS usually greater than 0.12 seconds because of bundle branch block. Often progresses to third degree block and has a poor prognosis. Reduced HR results in decreased CO with hypotension and myocardial ischemia. Permanent pacemaker is indicated. Atropine is not indicated for this dysrhythmia.
o A third-degree atrioventricular block is a complete failure of the AV node to conduct any impulses from the atria to the ventricles. This may be due to an AV nodal disease, enhanced vagal tone, a congenital disorder, and/or underlying structural heart diseases. This AV block requires clients to have a pacemaker inserted (ACLS, 2018).
2. Describe symptoms of a patient experiencing a myocardial infarction.
o The most common symptoms of a patient experiencing myocardial infarction include pressure or tightness in the chest; pain in the back, chest, jaw and other areas of the upper body that lasts more than a few minutes or that goes away and comes back; shortness of breath; diaphoresis; nausea; vomiting; anxiety; and/or a cough.
o Later BP may drop due to decreased CO
o This may result in decreased urinary output
o Crackles
o JVD, hepatic engorgement, peripheral edema
o Abnormal heart sounds (S3 and S4 or loud holosystolic murmur)
o Temperature increase
o (Macon, Yu, Reed-Guy, 2017).
3. Discuss safety implications during defibrillation.
o If a defibrillator gives a “shock advised” prompt, ensure that no one is touching the patient and loudly state “I’m clear, you’re clear, everyone clear!” (Furst, 2015)
o If water is present, use a towel to dry the patient’s chest – water and electricity don’t mix (Furst, 2015).
o Do not use the defibrillator in an explosive environment or in one where there is a buildup of flammable vapors (Furst, 2015).
o If oxygen is used, it should be at least one meter away from the AED (Furst, 2015).
o If the patient has excessive chest hair, shave off or rip off hair with the pads before inducing and electrical shock (Furst, 2015).
4. Review 2010 ACLS guidelines for treatment of third-degree heart block, PEA, and ventricular
fibrillation.
o Third Degree heart block
o Pharmacologic Treatments
Atropine: The first drug of choice for symptomatic bradycardia. The dose in the Bradycardia ACLS algorithm is 0.5mg IV push and may repeat up to a total dose of 3mg.
Dopamine: Second-line drug for symptomatic bradycardia when atropine is not effective. Dosage is 2-20 micrograms/kg/min infusion.
Epinephrine: Can be used as an equal alternative to dopamine when atropine is not effective. Dosage is 2-10 micrograms/min.
o TCP-transcutaneous pacing
o PEA
o Pharmacologic Treatments
Epinephrine can be given as soon as possible but its administration should not delay the initiation or continuation of CPR. High-quality CPR should be administered while giving epinephrine, and after the initial dose, epinephrine is given every 3-5 minutes.
o Ventricular Fibrillation
o Pharmacologic Treatments
Epinephrine is primarily used for its vasoconstrictive effects. Vasoconstriction is important during CPR because it will help increase blood flow to the brain and heart.
Amiodarone, lidocaine, and magnesium are antiarrhythmic medications that are used in the left branch of the Cardiac Arrest Algorithm
o Actions-
CPR performed until defibrillator is attached to pt
Interruptions in chest compressions kept to a minimum
Rapid use of defibrillator emphasized
Use manual defibrillator over AED (longer interruptions)
5. Discuss potential causes of PEA.
o Causes of potential PEAs can include many conditions but the most frequent causes are hypovolemia and hypoxemia. Internal bleeding should be considered as well with PEAs – this “hidden” hypovolemia may cause a PEA and may potentially be deadly
o Metabolic acidosis, hyperkalemia, hypokalemia, hypoglycemia, hypothermia, toxins (drug overdose), cardiac tamponade, thrombosis (MI, pulmonary emboli), tension pneumothorax, and trauma
o (ACLS, 2018)
6. If the patient would have been resuscitated, describe post-cardiac arrest care.
o Optimize ventilation and oxygenation by starting with 10 breaths a minute and using the lowest inspired oxygen concentration necessary to maintain a Sat of 94% or greater. Use continuous waveform capnography to confirm and monitor correct placement of the ET tube, if needed.
o Treat hypotension when BP is less than 90 – obtain IV access and treat hypotension with a bolus and vasopressor infusion. Obtain a 12-lead ECG. Transfer client to an appropriate facility if STEMI is detected.
o Initiate target temperature management and transfer client to an advanced critical care unit if STEMI or AMI are not detected
o (ACLS, 2018).
7. Discuss the ECG lead waveforms would you examine to determine an inferior, lateral,
posterior, or Interior MI.
o Inferior MI
o ST elevation in leads II, III, aVf
o ST depression in leads I, aVL, V5, and V6
o Lateral MI
o ST elevation in leads I, aVL, V5, V6
o ST depression in leads II, III, aVF
o Posterior MI
o ST elevation in leads V7-V9
o ST depression in leads V1-V4
o Anterior MI
o ST elevation in leads V2-V4
o ST depression in leads II, III, aVf
o (Ryan, 2012)
8. Differentiate UA, ACS, NSTEMI, and STEMI acronyms used in cardiac care.
o UA: unstable angina
o ACS: acute coronary syndrome
o NSTEMI: non-ST elevated myocardial infarction
o STEMI: ST elevated myocardial infarction
9. Discuss the reasons and assessment you would make when a patient’s heart rate suddenly increases from 88 to 120 beats per minute.
o You would assess a patient whose heart rate suddenly increases from 88 to 120 because a sudden increase in heart rate can cause sudden cardiac arrest. A heart rate over 80 bpm more often leads to atherosclerotic plaque which can lead to developing acute coronary syndrome and arrhythmias. (Davidovic et. al., 2013).
10. Discuss why patients with pulmonary disease are prone to atrial dysrhythmias.
o Patients with pulmonary diseases are prone to atrial and ventricular dysrhythmias. The pathogenesis is complex and involve many factors. Individuals may have anatomic cardiac abnormalities or other complications, such as, an atherosclerotic heart. Hypoxia and hypercapnia in some patients can be arrhymogenic as well (Prystowsky & Klein, 2013).
11. Discuss the treatment of a patient with a history of hypertension and coronary artery experiencing nausea and vomiting for 24 hours. When she is connected to the monitor, you note a heart rate of 50 beats per minute. Discuss the assessment data will you collect related to the bradycardia. Discuss questions will you ask during your nursing history.
• Treatment for a patient with hypertension and CAD:
o Reduce sodium intake
High sodium intake can contribute to hypertension
Sodium can decrease the effectiveness of certain antihypertensive medications
o Control blood sugars with diabetics
When hypertension and diabetes coexist, complications such as target organ disease are more severe
The incidence with CAD is 2-4 times greater among people with diabetes
o Watch for elevated serum lipids
Increased levels of cholesterol and triglycerides are primary risk factors for atherosclerosis (main cause of CAD)
Hyperlipidemia is more common in people with hypertension
o Stress may contribute to hypertension and CAD
o Hypertension is the second major risk factor in CAD
• Medications for Hypertension
o Diuretics
o Adrenergic-inhibiting agents
Act by diminishing the SNS effects that increase BP
Adrenergic inhibitors include drugs that act centrally on the vasomotor center and peripherally to inhibit norepinephrine release or to block the adrenergic receptors on blood vessels
o Direct vasodilators
Decrease BP by relaxing the vascular smooth muscle and reducing SVR
o Calcium Channel Blockers
Increase sodium excretion and cause arteriolar vasodilation by preventive the movement of extracellular calcium into cells
o Angiotensin-converting enzyme (ACE) inhibitors
• Medications for CAD
o Statins
Block synthesis of cholesterol and increase LDL receptors in liver
Decrease LDL and triglycerides
Increase HDL
o Niacin
Inhibits synthesis and secretion of VLDL and LDL
Decrease LDL and triglycerides
Increase HDL
• Bradycardia
o Can be caused by rest or sleeping, SA or AV node damage, athletic conditioning, side effects of drugs (beta blockers), or hypothyroidism
o Assessment:
Vital signs
Inspect for skin color
Check for edema, dependent rubor, clubbing of the nail beds, varsities, and lesions such as stasis ulcers
Inspect large veins in the neck
Palpate the upper and lower extremities for temperature, moisture, pulses
Palpate the pulses in the neck and extremities for information in arterial blood flow
Assess the rhythm and force
Capillary refill should occur in less than 2 seconds
o Ask patient about:
Chest pain or discomfort
Palpitations
Shortness of breath (laying down or at rest)
Edema in legs or body
Leg pain during exercise
Excess urination
o Treatment
Give IV atropine
If atropine is ineffective, transcutaneous pacing or a dopamine or epinephrine infusion is considered
o (Lewis, 2017)
12. Discuss why tachycardia sometimes leads to heart failure.
o Tachycardia-induced cardiomyopathy develops slowly and appears reversible by left ventricular ejection fraction improvement, but recurrent tachycardia causes rapid decline in left ventricular function and development of heart failure. Sudden death is possible (Nerheim, 2004).
13. A 65 year old woman is transported an unwitnessed full arrest to the ED. Active resuscitation is in progress-the patient has been defibrillated with 200j results in. The patient looks like she weighs 50 kg. What should you do now?
o Continue chest compressions, prevent hypothermia/hyperthermia, optimize hemodynamic and gas exchange, initiate coronary reperfusion, control glucose levels and assess neurological status
14. You are working in the emergency department and are called to the bedside of a patient who has suddenly become unresponsive. No pulse can be felt and the patient is having agonal breathing. The patient is middle age weighs 70kg.
A defibrillator and the code team is at the bedside. Quick look paddles are applied and reveal the rhythm show. How would you proceed?
o The patient is in ventricular tachycardia
o Defibrillate the patient
o Administer oxygen and prepare for intubation
o Give 300 mg IV push of amiodarone, if no conversion, Give 150 mg IV push
With intervention patient has a weak pulse and a palpated blood pressure of 60. The patient is still unresponsive what has happened?
o The patient now has a 3rd degree heart block
o The patient is hypotensive
o Give the patient IV fluids to help increase blood pressure
o Auscultate lung sounds to ensure the patient is not becoming fluid overloaded
o Patient may need vasoconstrictor such as norepinephrine (Levophed)
o Continue to monitor patient
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